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Arrb1 reduced the chemotherapy-induced Lgr5 (show LGR5 Proteins) stem cell apoptosis by inhibiting endoplasmic reticulum stress-mediated mitochondrial apoptotic signaling.
findings suggest that knockdown of beta-arrestin 1 can suppress glioblastoma multiforme cell proliferation, invasion and glycolysis by inhibiting Src (show SRC Proteins) signaling
Results revealed that beta-arrestin-1 regulates lactate metabolism to contribute to beta2-adrenergic receptor (show ADRB2 Proteins) functions in improved memory formation.
Study reports an X-ray free electron laser crystal structure of the rhodopsin (show RHO Proteins)-arrestin (show SAG Proteins) complex, in which the phosphorylated C terminus of rhodopsin (show RHO Proteins) forms an extended intermolecular beta sheet with the N-terminal beta strands of arrestin (show SAG Proteins). Phosphorylation was detected at rhodopsin (show RHO Proteins) C-terminal tail residues T336 and S338.
Beta-arrestin-1 with beta-arrestin-2 shared common mechanisms to suppress podocyte autophagy by negative regulation of ATG12-ATG5 conjugation.
data suggest that beta-arr1 mediated nuclear signaling regulates the production of excretive factors derived from niche astrocytes and expansion of neural precursors in DG, thus maintaining homeostasis of adult hippocampal neurogenesis
beta-arr1 (show SAG Proteins) has a critical role in modulating ERK (show EPHB2 Proteins), JNK (show MAPK8 Proteins) and p38 MAPK (show MAPK14 Proteins) pathways mediated by TNF-alpha (show TNF Proteins) in intestinal epithelial cells.
COX-2-derived PGE2 inhibits IL-10 expression in brain microglia through a novel EP2- and beta-arrestin-dependent signaling pathway.
A specific hyaluronan-blocking peptide (Pep-1 (show CNDP2 Proteins)) has confirmed the inflammatory role of degraded hyaluronan as a mediator of the IL-1beta (show IL1B Proteins)-induced activation of beta-arrestin-1.
Data suggest that ARRB1 enhances hepatocellular carcinogenesis by inflammation-mediated Akt (show AKT1 Proteins) signaling.
This work demonstrates that the expression of FSHR (show FSHR Proteins) and LHCGR (show LHCGR Proteins) can be induced in hGL5 cells but that the FSHR (show FSHR Proteins)-dependent cAMP/PKA pathway is constitutively silenced, possibly to protect cells from FSHR (show FSHR Proteins)-cAMP-PKA-induced apoptosis.
This study reveals contrasting abilities of IGF-1R (show IGF1R Proteins) to interact with each b-arrestin (show SAG Proteins) isoform, depending on the presence of the ligand and demonstrates the antagonism between the two b-arrestin (show SAG Proteins) isoforms in controlling IGF-1R (show IGF1R Proteins) expression and function, which could be developed into a practical anti-IGF-1R (show IGF1R Proteins) strategy for cancer therapy.
Lowering the level of cellular FLNA caused an elevation in RalA activity and resulted in selective interference with the normal intracellular trafficking and signaling of D3R through beta-arrestins.
the depleted beta-Arrestin1 reduced the interaction of P300 (show EP300 Proteins) with Sp1 (show PSG1 Proteins), thus to reduce Sp1 (show PSG1 Proteins) binding to hTERT promoter, downregulate hTERT transcription, decrease telomerase activity, shorten telomere length, and promote Reh (show CES1 Proteins) cell senescence.
Data show that endothelin A receptor (show EDNRA Proteins) drives invadopodia function by direct interaction of beta-arrestin-1 (beta-arr1) with Rho guanine nucleotide exchange factor (GEF) 11 (show ARHGEF11 Proteins) protein (PDZ-RhoGEF (show ARHGEF11 Proteins)).
The small GTPase (show RACGAP1 Proteins) Ras-related protein (show RASD1 Proteins) 2 (Rap2 (show RAP2A Proteins)) was found to bind ArrB1 under resting conditions but dissociated upon formyl-Met-Leu-Phe stimulation.
These results were consistent with those seen for beta2-AR. Thus, both beta-arrs negatively control AM1 receptor internalization, which depends on the C-tail of CLR (show DCLK3 Proteins).
Results indicate a mechanism of beta-arrestin1 in modulating epithelial-mesenchymal transition (EMT) and glycogen synthase kinase 3 beta (GSK-3beta)/beta-catenin signaling in prostate cancer, and suggest that assessment of beta-arrestin1 may provide a potential therapeutic target for prostate cancer.
Using in vivo time-lapse imaging and three-dimensional morphology analysis of microglia in intact zebrafish larvae, study found that beta-arrestin1, a multifunctional protein involved in various signal transductions, cell-autonomously regulated the microglial morphology.
Study demonstrated that beta-arrestin1 is critically involved in zebrafish primitive hematopoiesis, where beta-arrestin1 binds to and sequesters the PcG recruiter YY1 (show YY1 Proteins), thus relieving PcG-mediated repression of cdx4-hox (show MSH2 Proteins) pathway.
The identified receptor-phospho-selective mechanism for arrestin (show SAG Proteins) conformation and the spacing of the multiple phosphate-binding sites in the arrestin (show SAG Proteins) enable arrestin (show SAG Proteins) to recognize plethora phosphorylation states of numerous GPCRs.
The presented functional map quantitatively connects critical interactions in the polar core and along the C tail of arrestin (show SAG Proteins).
Reduced binding of arrestin-1 (show SAG Proteins) to the phospho-opsin (show RHO Proteins) form of G90D mutant likely contributes to night blindness caused by this mutation.
3.0 A crystal structure of the bovine arrestin-1 splice variant p44, in which the activation step is mimicked by C-tail truncation
Conformational dynamics of helix 8 in the GPCR rhodopsin (show RHO Proteins) controls arrestin (show SAG Proteins) activation in the desensitization process
similar to transducin (show GNAT1 Proteins) activation, rhodopsin (show RHO Proteins) phosphorylation by GRK1 (show GRK1 Proteins) and high affinity arrestin-1 (show SAG Proteins) binding only requires a rhodopsin (show RHO Proteins) monomer
Members of arrestin/beta-arrestin protein family are thought to participate in agonist-mediated desensitization of G-protein-coupled receptors and cause specific dampening of cellular responses to stimuli such as hormones, neurotransmitters, or sensory signals. Arrestin beta 1 is a cytosolic protein and acts as a cofactor in the beta-adrenergic receptor kinase (BARK) mediated desensitization of beta-adrenergic receptors. Besides the central nervous system, it is expressed at high levels in peripheral blood leukocytes, and thus the BARK/beta-arrestin system is believed to play a major role in regulating receptor-mediated immune functions. Alternatively spliced transcripts encoding different isoforms of arrestin beta 1 have been described.
arrestin, beta 1
, arrestin 1
, beta-arrestin 1
, arrestin beta 1
, arrestin beta-1
, arrestin 2